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Regular physical activity confers physiological, metabolic benefits

This is an excerpt from Physical Activity and Health-2nd Edition edited by Claude Bouchard, Steven N. Blair and William Haskell.


A healthy lifestyle offers numerous benefits. Find more of the latest research on the relationship between physical activity, sedentarism, and health in Physical Activity and Health, Second Edition.

Research has repeatedly shown that exposure to regular, frequent bouts of physical activity stimulates physiological and metabolic changes that benefit health. It is helpful to classify these as either (a) chronic effects, that is, adaptations to training acquired over weeks or months, or (b) short-term, acute responses to each individual session of activity. Health-related adaptations to training are dealt with in other chapters. This chapter describes selected acute responses that are clearly related to health outcomes and explains their relevance. The extent to which these responses benefit health depends on the type, frequency, and regularity of activity and the extent to which particular acute responses persist into the postactivity period. For people who achieve the minimum recommended amounts of physical activity (Haskell et al. 2007, p. 1423), acute responses should be stimulated on five days per week (for moderate-intensity activity) or three days per week (for vigorous intensity). For reasons often related to statistical power and logistical considerations, the experimental models used to study acute health-related responses have relied mainly on planned, structured exercise, as opposed to physical activity performed during daily living. For this reason, the term exercise predominates in this chapter rather than physical activity. Studies of short periods of detraining are included because they illustrate that the changes to health outcomes that are rapidly lost when regular training is interrupted are mainly attributable to acute effects. Intuitively, unstructured periods of physical activity may be expected to stimulate acute responses that are qualitatively similar to, but less conspicuous than, those arising from planned sessions of exercise.

Lipids and Lipoproteins

Lipoproteins are particles that transport triglycerides and cholesterol in the blood plasma. They have a hydrophobic lipid core and an outer surface layer that allows the particle to mix with the watery plasma. Lipoproteins are classified according to their density, which in turn reflects their composition (see “Characteristics of the Main Classes of Lipoproteins”). There are clear links between markers for disordered lipoprotein metabolism and heart disease: Plasma concentrations of total cholesterol, low-density lipoprotein (LDL) cholesterol, and triglycerides are positively associated with the incidence of coronary heart disease, and there is a clear inverse relationship between high-density lipoprotein (HDL) cholesterol concentration and heart disease incidence. Changes to the concentration of lipoprotein lipids arising from a session of exercise are therefore of interest because of their implications for cardiovascular risk.

When considerable amounts of energy have been expended, changes to plasma concentrations of triglycerides, total cholesterol, or HDL cholesterol may be observed immediately after an exercise session. For example, men and women who completed the 1994 Hawaii Ironman Triathlon exhibited a nearly 40% decrease in triglycerides and decreases of around 10% in total and LDL cholesterol compared with prerace values. Events such as a marathon can result in an increase in HDL of about 10% after the race. These changes are independent of changes to plasma volume during these endurance events. On the other hand, a session of moderate-intensity exercise of relatively short duration does not lead to clear changes in lipoprotein variables measured immediately afterward. However, these measurements do not reveal the extent of the influence of such an exercise bout on lipoprotein metabolism.

Even a modest session of activity makes important inroads into the body’s energy stores, leading to a prolonged period of metabolic “recovery.” Thus, when blood samples are obtained hours (rather than minutes) after exercise, effects on lipoprotein metabolism are clear. Decreases in triglycerides and increases in HDL cholesterol measured in the fasted state 24 h after a session of exercise have consistently been observed. The design of the HERITAGE Family Study was such that chronic adaptations to training could be distinguished from acute effects. In samples obtained 24 h following the last exercise session, researchers found that total cholesterol and very low-density lipoprotein (VLDL) triglycerides were lower after 20 weeks of training than at baseline, but there were no changes in samples obtained 72 h posttraining. In other words, these reductions were clearly acute responses to the last bout of exercise. The main factor influencing the extent of acute changes to triglycerides and HDL is the amount of energy expended during the exercise session, irrespective of exercise intensity. It may be that around 4.2 MJ (1,000 kcal or the equivalent of walking more than 16 km [10 mi]) need to be expended to elicit statistically significant changes.

These changes reflect the functional relationship that exists between plasma concentrations of triglycerides and HDL cholesterol. Hydrolysis of triglyceride-rich lipoproteins (chylomicrons and VLDL cholesterol) by the enzyme lipoprotein lipase (LPL) is accompanied by the transfer of cholesterol and other surface materials from triglyceride-rich particles into HDL. Thus, rapid removal of triglyceride-rich lipoproteins is associated with an increase in cholesterol carried in HDL. Prior exercise enhances triglyceride clearance rates, probably by increasing the activity of LPL in muscle—the rate-limiting step in triglyceride clearance. However, there appears to be little cumulative effect of repeated daily sessions of exercise on LPL activity, explaining why the decrease in triglycerides is essentially an acute effect of exercise that dissipates within 24 h.

Effect of Prior Exercise on Postprandial Triglycerides

Changes to lipoprotein metabolism after an exercise session therefore derive mainly from enhanced clearance of triglyceride-rich lipoproteins, a phenomenon most clearly seen when these particles are most numerous, that is, during the postprandial state. A rich body of data illustrates that prior exercise markedly decreases the triglyceride response to a subsequent meal. The clinical relevance of this is that an exaggerated postprandial triglyceride response has been linked to the presence of coronary artery disease and to the atherogenic lipoprotein phenotype. Moreover, people spend the majority of their lives in the postprandial state.

Figure 6.1 shows the effect of afternoon exercise (90 min at 60% of .VO2max) on serum triglyceride concentrations during the 6 h following a standard, high-fat meal consumed the following morning. The subjects were normally active (figure 6.1a) and endurance-trained (figure 6.1b) middle-aged women (Tsetsonis, Hardman, and Mastana 1997). Prior exercise decreased the postprandial response, measured as the area under the triglyceride concentration versus time curve, by 30% in trained women and by 16% in normally active women compared with values obtained in the control trial (no planned exercise for three days beforehand). Thus, a single session of exercise markedly decreases subsequent postprandial lipemia. This effect has been confirmed in various subject groups, including the obese. However, even in trained athletes, this effect is short-lived—and therefore an acute effect—as shown by a study of detraining. Endurance-trained athletes consumed a test meal on three occasions: 15 h, 60 h, and 6.5 days after their last training session. Compared with the 15-h value, the postprandial triglyceride response was 35% higher after just 60 h without exercise, with little further increase after nearly a week without training. Frequent exercise is therefore needed to maintain the cardiovascular benefits that may be assumed to arise from the triglyceride-lowering effects.

Influence of Intensity and Duration

Prior exercise has such a clear effect on postprandial triglycerides that this model has allowed investigation of the influence of exercise intensity (figure 6.2) and pattern (figure 6.3). Researchers examined the effect of the intensity of prior exercise (controlling for energy expenditure) using a repeated-measures design (Tsetsonis and Hardman 1996). The same participants consumed a high-fat, mixed meal on three occasions: (1) control, no planned exercise for three days beforehand; (2) 15 h after a 90-min treadmill walk at 60% .VO2max; and (3) 15 h after a walk that was twice as long (180 min) but at half the intensity (30% .VO2max). In other words, the researchers asked, “Can intensity be ‘traded’ for duration?” As figure 6.2 clearly shows, the postprandial triglyceride response to dietary fat was decreased to the same degree (32%) after both exercise sessions, so the answer to this question (for this particular health outcome) is yes.

Different patterns of walking were compared in a study of daylong plasma triglyceride concentrations (figure 6.3). On three occasions, middle-aged participants were followed throughout a day during which they consumed three ordinary meals (Murphy, Nevill, and Hardman 2000). Compared with values from a control trial in which participants sat and worked quietly, plasma triglyceride concentrations were decreased to the same degree (12%) by either one 30-min walk before breakfast or by three 10-min walks taken before breakfast, lunch, and the early-evening meal. A subsequent study that compared the effect of 30 min of continuous walking with that of ten 3-min bouts reported strikingly similar findings (Miyashita, Burns, and Stensel 2008). Thus, the acute decrease in postprandial triglycerides attributable to exercise appears to be determined by the associated energy expenditure rather than by its intensity or pattern. Finally, there is evidence that the triglyceride-lowering effect of a bout of exercise extends into “real-world” settings where there may be a compensatory increase in food intake that reduces the net energy deficit attributable to the exercise bout (Farah, Malkova, and Gill 2010).

Endothelial Function

As mentioned previously, changes to lipoprotein metabolism during the hours after meal ingestion are likely to play an important role in the atherosclerotic disease process. However, the postprandial state is characterized also by nonlipid disturbances that are central to the progression of atherosclerosis.

Studies using a repeated-measures design have been employed to examine the effect of prior exercise on the postprandial impairment of endothelial function that persists for many hours after a high-fat meal. For example, using laser Doppler imaging of vasodilator responses to acetylcholine, researchers found that prior moderate exercise (90 min at 50% .VO2max) improved endothelium-dependent vasodilator function by an average of 15% over an 8-h postprandial period (Gill et al. 2004). This technique assesses the cutaneous microcirculation, regarded as a robust surrogate marker of vascular function in other vascular beds more directly involved in the pathogenesis of vascular diseases. Using a different technique, Tyldum and colleagues (2009) found significant attenuation by a single session of moderate exercise of the decrement in flow-mediated vasodilation of the brachial artery associated with a high-fat meal.

Improvements to endothelial function after a single exercise session appear therefore to be clearly discernable in small studies of apparently healthy subjects. Future repeated-measures studies to examine variables of duration, intensity, and pattern are feasible, as well as studies in groups that differ in clinical or training status. Complementary work will no doubt address the mechanisms by which exercise ameliorates postprandial impairment of vascular function: One possibility is a reduction by exercise of postprandial levels of oxidative stress.

Insulin–Glucose Dynamics

Insulin resistance is the main pathology of type 2 diabetes, and skeletal muscle is the body’s largest insulin-sensitive tissue (see chapter 13). It is not surprising, therefore, that substrate deficits arising from a session of exercise influence whole-body insulin–glucose dynamics.

It has been known since the 1970s that endurance-trained individuals exhibit normal or improved glucose tolerance to a carbohydrate challenge despite a markedly reduced insulin response. More recently, a raft of detraining studies has shown that the improved insulin action underlying these characteristics is rapidly reversed with inactivity, suggesting that much of this benefit arises from acute rather than chronic effects. For example, King and colleagues investigated the effects of a seven-day interruption to training on glucose tolerance and insulin action (King et al. 1995). Participants were middle-aged individuals with a habit of regular moderate exercise, and the measures used were derived from a simple oral glucose tolerance test (OGTT) so as to reflect normal homeostatic mechanisms that pertain to real life. During the five days before these tests, participants performed 45 min of exercise daily at about 70% .VO2max. Glucose tolerance was poor immediately after the last exercise session, possibly because elevated plasma concentrations of nonesterified fatty acids inhibit glucose uptake into muscle, but had improved markedly 24 h later. This improved insulin action persisted for three days but not for five days, suggesting that the frequency of exercise needed to maintain the exercise-induced improvement in glucose tolerance is once every three days (figure 6.4). These findings were confirmed by the HERITAGE study of more than 500 previously sedentary men and women; 24 h after the last exercise bout of a 20-week training program, fasting insulin concentrations were lower than at pretraining, but this improvement was no longer evident 72 h after the last bout.


Read more from Physical Activity and Health-2nd Edition edited by Claude Bouchard, Steven N. Blair and William Haskell.



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